“Junin arenavirus infection enhanced by DC-SIGN C type lectin. Preliminary studies”

IULA LJ; MARTINEZ G; CANDURRA NA; CORDO SM.

Congreso; First French-Argentine Immunology Congress; 2010

Sociedad Argentina de Inmunologia y Sociedad Francesa de Inmunologia

@font-face { font-family: "Times New Roman"; }@font-face { font-family: "Arial Narrow"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0in 0in 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }table.MsoNormalTable { font-size: 10pt; font-family: "Times New Roman"; }div.Section1 { page: Section1; } Abstract Cell tropism of enveloped viruses is regulated by binding of viral envelope glycoproteins to specific cell-surface receptors which determines susceptibility at a host cell, tissue or species level. However, a number of additional cell-surface moieties can also bind viral envelope glycoproteins and could act as capture receptors, serving as attachment factors to concentrate virus particles on the cell surface to disseminate the virus infection to target organs or susceptible cells within the host. Junin virus (JUNV) is a pathogenic member of the Arenaviridae family and it has been shown that transferrin receptor function as its cellular receptor specifically binding to the viral glycoprotein. In addition previous experiments using relatively non-permissive mouse 3T3 cells showed that they became significantly more susceptible to JUNV when the cells expressed DC-sign, been blocked by addition of mannan or anti–DC-sign antibodies. We aim to investigate the role of C-lectins on JUNV infection. Transmission mediated by DC-sign expressing cells was studied for HIV and others viruses. In this preliminary report we used Raji or Raji DC-sign expressing cells to explore the ability of this cells to mediate cell-cell JUNV transmission. Incubation of JUNV with Raji cells resulted in a productive infection with maximum titer in supernatants on day 21 post-infection. Conversely cells expressing DC-sign showed similar yields already on day 5. On the other hand, in both Raji and Raji DC-sign cell-associated infectivity was 2 log higher than in supernatants. In co-culture assays Raji cells were infected and then incubated with Vero cells. We measured infected Vero cells at different times by indirect immunofluorescence with the Raji ability to produce infectious centers on Vero cells was also examined. Our study shows that Raji linfocitic cell line could be infected by JUNV and that the presence of DC-sign lectin notable increases the chance of infection and cell transmission.